Electromagnetic radiation treatment for cancer and pathological genetic regulations

ABSTRACT

An electromagnetic radiation treatment regime includes identifying a target area of a patient that comprises at least some cancer cells, or other cells amenable to pathological genetic regulations. An electromagnetic radiation source, for example, a low frequency and/or radio frequency electromagnetic radiation source, is selected, along with treatment session parameters, such as, pulse frequency, pulse duration, electrical current, magnetic flux density, and/or treatment session exposure time. An amount of electromagnetic radiation is applied to the target area, and a response to the electromagnetic radiation by at least some of the cancer cells in the target area is measured. Based on an evaluation of the measured response, the treatment parameters may be modified for one or more subsequent electromagnetic radiation treatment session.

BACKGROUND OF THE INVENTION

1. Field of the Invention

Low frequency electromagnetic radiation and radio frequencyelectromagnetic radiation are applied separately or in combination withone another to a target area of a patient, wherein the target areaincludes at least some cancer cells, or other cells amenable topathological genetic regulations. The electromagnetic radiation altersthe control system of at least some of the cells forcing them to returnto a normal cellular control system, and/or the electromagneticradiation serves to promote apoptosis or cell death in at least some ofthe cells, with little to no affect on the surrounding normal cellpopulation.

2. Description of the Related Art

Cells contain mechanisms that regulate and control their variousactivities, among these are the control mechanisms that maintain propergrowth rates of a cell, as well as the timing of cell death, whenappropriate. Normal cells grow or replicate in response to an externalsignal, such as a growth factor that acts on an extracellular membranebound protein, initiating a signaling cascade that ultimately leads tocell growth. For example, nerve growth factor, platelet derived growthfactor, and epidermal growth factor, represent three such factors. Thus,growth in a normal cell is externally regulated and includes animportant external input.

Normal cells also include mechanisms which control programmed celldeath, or apoptosis. It is important that cells die off in order tolimit the number of genetic mutations in a population of cells, whichoccur more frequently with increased cell divisions, as well as to keeptissues and organs functioning properly.

A number of factors contribute to the control and orchestration of cellgrowth, as well as cell death. Perhaps the most basic of these isdeoxyribonucleic acid (“DNA”). DNA is a complex biomolecule comprised ofa series of corresponding base pairs of nucleic acids. These base pairsmay have positive or negative charges, which therefore render positiveor negative charges at various points along the DNA molecule. Due inpart to the charge distribution, DNA can assume a number of shapes orconformations depending on the quantity and movement of charge in thebiomolecule. For instance, DNA can be in a linear conformation with anegative charge in its base pairs, thereby forming double helix as isthe case with nuclear DNA. It can also be in a circular form, such as inmitochondrial or bacterial DNA. Thus, DNA comprises the building blocksfrom which cells are formed.

Moreover, DNA contains the genetic information of the cell, and must becopied or replicated each time the cell divides. Similarly, DNA strandsmust be separated and sorted into dividing cells during mitosis, i.e.,growth, and meiosis, i.e., reproduction, in order to convey the geneticinformation to the next generation of cells. Therefore, these processesalso affect the rate of cell growth, and the conformation of the DNAmolecule affects the replication, mitosis, and meiosis processes.

Microtubules also affect cell growth. A microtubule is a hollowcylindrical polymer dipole with its negative pole at the centrosome ofthe nucleus of a cell and its positive pole at the cell membrane.Microtubule growth occurs at the positive pole at the cell membrane, andtherefore can be said to radiate out from the centrosome. Accordingly,microtubules connect the cellular membrane to the nucleus of a cell.Microtubules are also used within the nucleus to guide separating DNAstrands during mitosis.

Energy drives the many processes in a cell, including growth, DNAreplication, mitosis, and meiosis. The cell is a self regulating systemwhere the functions are regulated within the energy level required. Morein particular, the cellular control system sets the level of energyrequired for a specific function of the cell. This energy, in the formof adenosine triphosphate, or ATP, is synthesized in the mitochondria ofthe cell.

A proton driven ATP synthesis is a critical mechanism of the cellularcontrol system. Specifically, the electron transport chain is a seriesof proteins associated with the mitochondrial membrane that transferelectrons stepwise between the proteins. Simultaneously, protons arepumped against an electrochemical gradient to the exterior of themembrane. Energy is temporarily stored in this proton gradient. Uponflowing back through the inner membrane, these protons are acted upon bythe membrane bound enzyme ATP synthase to relinquish this energy to ATP,an energy storage mechanism which stores this energy in phosphate bonds.

The protein cytochrome C is an important component of the electrontransport chain located in the inner mitochondrial membrane. Rather thanbeing membrane bound, cytochrome C is loosely associated with the innermembrane by covalent bonds and flows along the inner membrane.Furthermore, cytochrome C has a heme group containing iron that allowscytochrome C to transport electrons between proteins. It is a centralcomponent of the electron transport chain and ATP synthesis.

Significant energy is produced through ATP synthesis mediated by theelectron transport chain. For instance, the protons pumped across themembrane exert an electrochemical gradient reaching about 60 to 100milliVolts (“mV”). This is in addition to the normal potential acrossthe membrane of about 140 mV. Accordingly, at its maximum, the totalpotential is in a range of about 200 to 240 mV. Moreover, with a lowproton gradient, electron transport occurs at a maximum rate, while anincrease of the proton gradient causes a decrease in electron transport.Thus the magnitude of the electrochemical gradient can affect both therate and direction of the electron transport, in turn determining theamount of ATP generated.

Cellular energy production does not change gradually or continuously,but jumps between different levels, wherein different levels of energyare required to perform different cellular functions. For instance, theelectron transport chain can operate to produce energy at a basic level,such as to maintain resting membrane potentials, etc., or jump to a newlevel as required for meiosis and cell division, etc., or jump to afunctional level for secretion, contraction, etc. Once the energy isproduced, it is stored in the phosphate bonds of ATP.

The discharge of energy from ATP can be accomplished by hydrolyzing theenergy rich phosphate bonds. A first hydrolysis step reduces ATP toadenosine diphosphate, or ADP. A subsequent step reduces ADP toadenosine monophosphate, or AMP. A further step reduces AMP topyrophosphate. Each of these steps hydrolyzes one phosphate bond,releasing significant energy to be utilized by the cell in various ways,such as to maintain membrane potential, enzymatic activity, proteinsynthesis, mitosis, etc. Corresponding with each hydrolysis step is adecrease of the electric charge of the molecule as ATP has a negativeelectric charge of four; ADP, three; AMP, two; pyrophosphate, one.

Proteins also affect the rate of cell growth and death. For instance,proteins are critical to a variety of cellular processes, including ATPsynthesis, signal transduction, cell division, secretion, etc. Proteinsare comprised of a series of amino acids and assume three dimensionalconformational shapes. Moreover, proteins may have positive or negativecharges appearing at various points in the molecule, often in relationto amino- or carboxyl-groups or charged side chains. For example, in thecircular form of a molecule, there may be a negative charge at one poleand two positive charges at the other pole, the charges themselves,being attractive, contribute to a circular form of the molecule. Forinstance, the amino acids glutamine and arginine, at each pole, canassume this charge of positive and negative.

Complex proteins can assume any of at least three (3) energy states,namely, from lowest to highest: linear; circular; or twisted. A possibleintermediate horseshoe form exists between linear and circular inenergy. As a result of charge differential over the molecule, membraneproteins are dipoles which can turn and twist under electric fieldchanges to the membrane potential. These molecules can be linear orcircular, horseshoe or twisted in their conformation, each having acorresponding electrochemical state. Depolarization of the membrane canchange the conformation of the protein to an active state, such as froma linear to a circular conformation. Associated with the twisted form ofthe protein is a distribution of negative and positive charges along themolecule which represents the highest energy state of the molecule, andthus, when the molecule changes conformation into the circular form, asignificant amount of energy is released.

Conformational changes of membrane bound proteins can be affected by themembrane potential, as is evidenced in the example of the Na⁺/K⁺ voltagegated ion channel. Specifically, there is a net amount of potassium ion(K+) inside the cellular membrane and a net amount of sodium ion (Na+)outside, wherein the membrane is permeable to potassium ion (K+), but isimpermeable to sodium ion (Na+). In nerve and muscle cells, when themembrane is depolarized upon the application of electric current, thevoltage gated ion channel is activated, initiating an action potentialacross the membrane and inducing a conformational change in the voltagegated ion channel, which in turn allows sodium ion (Na+) to enter thecell. The subsequent flow of potassium ion (K+) across the membranerepolarizes the membrane, to a potential in the range of approximately50 to 100 mV.

There are many types of membranes within a cell, each having a membranepotential. The membranes include the cellular outer membrane, themitochondrial inner and outer membranes, and the nuclear membrane. Thecellular membrane can be described as a lipid bilayer with a mosaic ofprotein impregnations or imprints. Here, the membrane potential isestablished by a negative charge on a protein whose hydrophilic endprojects into the interior of the cell. This potential determines themovement of ions and molecules across the membrane, such as discussedabove for potassium ions (K⁺) and sodium ions (Na⁺). However, it is alsopossible that protons (H⁺) also move across the membrane, as aconsequence of electron transport as described above in relation to ATPsynthesis at the mitochondrial membrane. The membrane of themitochondria involves the control of metabolism, mainly oxidative, byits potential, and ATP synthesis via electron-proton transport. Thenuclear membrane, in the interior of the cell, contains the DNA of thecell within its boundary.

The lipid bilayer of a cellular membrane is interspersed with proteinsof various composition and function which are charged, such that theyhave a dipole moment. Although all cells have a membrane potential ordipole moment, studies on membrane potential have been essentiallylimited to muscle or nerve cells where changes in the membrane potentialare the result of an electrical signal. In muscle cells, this electricalsignal initiates contraction of the muscle. In nerve cells, thiselectrical signal initiates the transmission of neurotransmittersbetween neurons.

Although all cells exhibit electrical properties, this has beeninvestigated seriously only in nerve, brain and muscle cells, and theaction potential is the predominant observation. All cells have amembrane potential, but only nerve and muscle cells are able to producean action potential which is both a signaling and activating mechanism.The action potential normally is initiated at one end of a nerve ormuscle cell by a depolarization of the membrane, resulting in areduction of the magnitude of the potential. At a certain point ofdepolarization, called threshold, the action potential is discharged andis self propagated to the other end of the cell to end in a synapse orjunction, where it generates a depolarization called a synapticpotential. The depolarization causes the release of a neurotransmitterwhich diffuses across the synaptic gap to depolarize the postsynapticcell body (which contains the nucleus, mitochondria, ribosomes, etc.),to produce an action potential in the postsynaptic cell which can repeatthis process.

The nerve cell, or neuron, may be either excitatory or inhibitory. Theexcitatory neuron acts as previously described to produce adepolarization. On the other hand, the inhibitory neuron releases aninhibitory neurotransmitter which acts to hyperpolarize the postsynapticcell body, creating an increase in the magnitude of the membranepotential and can prevent activity or an action potential in thepostsynaptic cell.

Changes in the cellular membrane potential of a postsynaptic cell cancause a change in the genetic material within the nucleus of that cell.For example, the action potential impacting the cell body of a neuron,or nerve cell, produces a depolarization which activates the FOS genewhich is related to growth and regulation. FOS is also a knownproto-oncogene, meaning that an appropriate virus can transform it intoan oncogene, thereby initiating a cancerous process.

There are relevant functions which membrane polarization regulates. Forinstance, in the neuronal membrane, polarization results in theswitching on of the action potential, also referred to as depolarizationof the membrane to threshold. The membrane acts as a semiconductor wherecurrent can be turned on or off, wherein the transport system or otherfunction can be turned off by hyperpolarization of the membrane.

Although the membrane potential is a Donnan or electrochemicalequilibrium potential, it requires an appreciable amount of energy tomaintain it. To maintain the membrane potentials, mitochondrial energyproduction is needed to synthesize ATP, which is used as the energysource separating ions across the membrane and maintaining the membranepotential. For example, the inner membrane of the mitochondria maintainsa membrane potential of about 140 mV as a result of the Na+/K+ voltagegated ion channel. However, the membrane potential can increase anywherefrom about 60 to 150 mV due to the accumulation of protons on thecytoplasmic side of the membrane, for a total potential in the range ofabout 200 to 290 mV. Accordingly, a significant amount of energy isrequired by the cell to maintain membrane potentials, as well ascellular processes within the cell that keep the cell functioningnormally.

Unlike normal cells, abnormal cells do not possess the normal cellularcontrol mechanisms and instead exhibit, among other things, uncontrolledcell growth and immortality. For instance, abnormal cells may havegenetic mutations, such as gene deletions, additions, point mutations,etc., that result in the interference of normal cell functioning andprocesses. This is the case in cancer cells, as well as cells infectedwith a virus such as H1N1 influenza, more commonly referred to as swineflu, or human immunodeficiency virus (“HIV”). Moreover, cancer cells andvirally infected cells share some of the same fundamental components andmechanisms.

One of the features common to abnormal cells such as cancer cells andvirally infected cells is an uncontrolled growth rate. For instance, thecancer cell appears to have an almost constant signal to grow andreproduce. Specifically, growth or reproduction of the cancer cell is aresult of a signal to grow and reproduce that is internally generated bythe cancer cell. In other words, the cancer cell can grow in the absenceof outside or external signals. This is in stark contrast to normalcells which grow and divide only in response to an external signal suchas a growth factor. Accordingly, growth of cancer cells is entirelyinternally regulated and independent of the limitations of itsenvironment, and therefore can grow continuously. Indeed, thisuncontrolled growth is a major factor contributing to the production oftumors in cancer tissue.

A cancer cell's development can be broken into two phases, wherein thecancer cell behaves differently in each phase. The first phase is calledinitiation or promotion, and occurs when the cancer cell is firstinitiating and developing. This phase is generally accepted to bereversible. The remaining phase of the cancer cell's development iscalled progression and is considered to be irreversible. During thisphase, the cancer cell propagates and proliferates, and can lead to thegrowth of tumors, invasion of neighboring tissues, and even metastasisto distant parts of the body. In order for the cancer cell tometastasize, it must break away from its adhesion to adjacent cells orthe extracellular matrix and enter the blood or lymph stream. Then thecancer cell eventually adheres to another tissue, organ, or cellularstructure.

In a number of aspects, including growth, an infected cell actssimilarly to a cancer cell, except that the progeny are viruses ratherthan cells. Once inside a host cell, viral DNA is integrated into thehost cell DNA through a process called transgenesis. Depending on thepoint of insertion, transgenesis may inactivate a tumor suppressor genewhich repairs damage, and therefore, renders the cell incapable ofrepairing damage. This can lead to increased incidence of geneticmutations and, ultimately, cancer in the cell. A similar result mayoccur from infection by an oncogenic virus, which induces cancerous typegrowth in the cell. Regardless of the method of transgenesis, onceintegration of viral DNA into the host genome is complete, the virusinduces the host cell to continuously replicate, thereby alsoreplicating the viral DNA. This replication occurs until the cellbursts, releasing a multitude of virus molecules into the body. Indeed,this is the goal of the virus, allowing its genes to propagatethroughout a host organism. Importantly, the signal to replicate comesfrom the virus itself, and therefore, similar to a cancer cell, it isinternally controlled. Since it does not rely on external factors forgrowth, the virally infected cell can continue to grow continuouslyuntil the cell bursts. Thus, the cancer or infected cell supersedes thecontrol system of the normal cell regarding growth.

Apoptosis, or programmed cell death, is also a part of a normal cell'scontrol system. Abnormal cells, such as the cancer cell and virallyinfected cell, no longer have a signal to initiate apoptosis and,therefore, these cells do not die off, rather, they become immortal.

Cellular structures and molecules are known to exhibit electrical andmagnetic properties. For example, as previously discussed, moleculessuch as proteins and DNA can have charged regions or components, whetherpositive or negative, which contribute to the electrical activity of themolecule. Membranes also have electrical properties as a result of theelectrochemical potential established and maintained by the presence andmovement of ions around and across the membrane. As mentionedpreviously, most of the information concerning electrodynamics of thenormal cell has been obtained from studies of nerve and muscle cells.

Cellular structures and molecules also exhibit magnetic properties. Forinstance, the protons within nuclei of cells are responsive to amagnetic field. Since each proton is a dipole, it will align or spin ina particular direction, either up or down, when placed in a magneticfield. Placing a cellular sample in a steady state magnetic fieldresults in the orientation of the protons of the cellular sample so theyspin in the same direction, i.e., all up or all down. Application of amagnetic pulse, 90° out of phase, excites the protons of the nuclei andforces the protons into the transverse plane. Subsequent to theapplication of the magnetic pulse, the protons return to their originalposition generated by the steady magnetic field, known as relaxation.This relaxation has a characteristic time constant, or duration ofexcitation, unique to each cellular sample type. For instance, the timeconstant is different for different types of tissues of the body, andthe time constant for cancer tissue is different than for non-canceroustissue of the same type. Fluids have a relatively long time constant, inthe range of about 1,500 to 2,000 milliseconds (“ms”), whereas watercontaining tissues have a time constant of about 400 to 1,200 ms, andfatty tissues have a shorter time constant in the range of about 100 to500 ms.

Thus, protons in different tissues of the body have different periods ofexcitation duration, or time constants. An example of this is presentedin Table 1 below showing the excitation times of proton populations foreach of two different magnetic flux densities, 0.5 Tesla (“T”) and 1.5T:

TABLE 1 Proton Population 0.5 T 1.5 T Spleen 760 ms 1,025 ms Liver 395ms 570 ms Fat 192 ms 200 ms Muscle 560 ms 1,075 ms CSF — 2,060 ms GreyMatter (Brain) 780 ms 1,100 ms White Matter (Brain) 520 ms 560 ms

Moreover, the Larmor frequency (r/2_(π)B), which relates to the angularmomentum of a spinning or precessing proton, for excitation of a proton(H⁺) increases with an increase of the magnetic field, or magnetic fluxdensity. For example, at 0.15 T it may be 6.39 MHz; at 0.5 T, 21.29 MHz;at 1.5 T, 63.87 MHz; at 3.0 T, 127.74 MHz.

To date, the utilization of the electrical and magnetic properties ofcellular components and molecules to affect changes in a cell have beenessentially limited to cardiac pacemakers or defibrillators, themagnetic stimulators, and the magnetic resonance imaging (MRI).

The cardiac pacemaker is used therapeutically to deliver an electricalcurrent or voltage directly to the heart muscle cells, usually those inthe ventricle, in order to correct fibrillation or tachycardia.Specifically, the rate at which the heart pumps blood is controlled bythe medulla in the brain which sends signals via sympathetic andparasympathetic nerves to the SA node of the heart to modulate thenodes' oscillatory depolarizations, thus producing the heart rate. Ifthe heart rate becomes too high, as in the case of tachycardia,fibrillation may result, which is characterized by groups of ventricularmuscles contracting independently of the SA node and each other, orasynchronously, resulting in a negligible blood pressure. Thedefibrillator corrects this by temporarily stopping the heart with anintense electric shock, after which, the heart should return to itsnormal rhythm. The pacemaker therefore utilizes the electricalproperties of cells and neuronal signaling to effect a change in thebody.

The magnetic stimulator, such as manufactured by MagStim and Danntec,has been used for diagnostic purposes, rehabilitation and psychologicalresearch. Essentially, the magnetic stimulator delivers current orvoltage to nerve cells, either in the brain or peripherally, via amagnetic field to depolarize motor cortex neurons and measure nerveconduction time. This involves the use of magnetic coils placed over atarget area to produce a pulsed magnetic field, thereby inducing anelectric field and resulting in an electrical current applied to atargeted area of the brain. Despite the use of a magnetic field togenerate an electrical current, the magnetic field is not directlyutilized for therapeutic purposes.

Magnetic resonance imaging (“MRI”) utilizes an EMR field applied toselected regions of the body for the purpose of producing an image. Toaccomplish this, magnetic fields are applied to specific regions of thebody in order to excite particular cellular components, such as protonswithin molecules or nuclei of cells. The excited protons or nuclei thenrelease this excess energy and return to equilibrium levels via theprocess of relaxation, and the time required for this return toequilibrium is known as the relaxation time. Raymond Damadian discoveredin the early 1970's that the relaxation time of cancer cells isdifferent from the neighboring normal cells, and thus the presence ofcancer can be determined and its magnitude observed. Accordingly, MRIutilizes the EMR properties of cells to provide an image of the tissueor organ, however, it does so based upon the magnetic properties ofcells, without utilization of the electrical currents induced by the MRIequipment itself.

Despite the fact that medical technology has utilized both electricaland magnetic properties of cells, cellular components and moleculesindependent of one another, no known medical technology simultaneouslycontrols and utilizes both electrical and magnetic properties fortherapeutic treatment purposes.

The interrelation between electric and magnetic properties of cells maybe observed. For example, when tissues or organs or body parts areexposed to a changing magnetic field, an electric field is producedwhich causes a current based on ionic movement. Positive and negativeions move in opposite directions, similar to the interior of an electricbattery. Accordingly, there is energy imparted by the magnetic field.For example, according to quantum mechanics, there are only two possiblestates of a proton (H⁺), with values of ±½, corresponding to whether theproton is in the spin up or spin down direction. The energy (E) of eachstate is:E=μB=rhI·Bwhere B is the magnetic field, h is Planck's constant, μ is the angularmomentum, r is the gyromagnetic ratio, and I is the angular momentumquantum value (½ for protons).

Present treatment regimens for cancer patients include surgery,chemoradiation, and pharmaceutical drugs, which are directed primarilyto the removal or eradication of the cancer cell population. However,these methods can not be limited solely to the cancer cell population,and as a result, normal healthy cells are also removed and/or eradicatedin the process.

For example, surgery has been a common technique for combating cancer,and is often used for the removal or excision of tumors. However, thereare significant risks involved with surgical treatment, as with anysurgery, including possible complications, hemorrhaging, adversereactions to aesthesia, etc. Moreover, surgical removal of cancer cellsis only feasible once the cancer has grown to a substantial population,and can therefore not be implemented for precancerous or early stages.While precancerous cells exhibiting abnormal characteristics can besurgically removed in order to avoid the development of cancer, thisoften involves removal of surrounding normal healthy tissue as well.Further, surgery may not be practical for the treatment of other formsof abnormal cells, such as those infected with a virus.

Chemoradiation has also been used to treat cancer. The main problem withthis therapy is safety. Chemoradiation involves subjecting tissue totoxic levels of radiation, which is intended to damage the DNA of thecells within the irradiated tissue, and thereby prompt cell death.However, this is a highly risky procedure as it is difficult to isolatejust the cancer cells, and so the surrounding healthy tissue cells arealso irradiated, damaged, and die. Because of its safety problems andlack of specificity, chemoradiation can only be utilized a limitednumber of times. Moreover, the cancer cell can mutate to becomeresistant to chemoradiation, further complicating treatment. Similarproblems would be encountered if chemotherapy or chemoradiation wereused to treat other abnormal cells, such as virally infected cells.

Cancer research, and in particular, research guided by the NationalInstitute of Health, has been aggressively pursuing pharmaceuticaltreatment regimens since the discovery of the first significantanticancer drug, cis-platinum over fifty years ago. However, the resultshave not been particularly significant given the effort and fundinglevels directed to this research. For example, although a number of newanticancer drugs have been developed by pharmaceutical companies, theyhave not succeeded in significantly increasing present levels ofeffectiveness which, with few exceptions, have improved only minimallyover the past fifty years. Also, most if not all pharmaceuticals fortreating cancer produce significant adverse side effects. This is alsothe case for many of the antiviral drugs on the market. Thus, it appearscritical to develop a new treatment regimen that could complement, ifnot replace altogether, present treatment regimens. It would besignificantly beneficial for such a new treatment regimen to comprisenone of the harsh and often detrimental side effects of known treatmentregimens.

It is evident that known treatment regimens for cancer cells arenon-specific, and equally and adversely impact all cells, normal andabnormal, in an affected area. More in particular, the known treatmentregimens involving chemoradiation and/or pharmaceuticals are highlytoxic to all cells and produce significant adverse side effects, andknown treatment regimens requiring surgery involve removal of healthycells along with target cancer cells. In any case, the known treatmentregimens for cancer cells are simply not completely effective.Accordingly, the medical community needs a safe and effective treatmentregimen for cancer cells.

SUMMARY OF THE INVENTION

The present disclosure is directed to a method for treatment of cancercells and pathological genetic regulations of other cells withelectromagnetic radiation. The present method includes identifying atarget area comprising a plurality of target area cells, wherein atleast some of the target area cells comprise cancer cells. In at leastone embodiment, the method also includes isolating the target area,however, it is envisioned that in at least some applications, the targetarea will include the entire body of the patient, in which case,isolation is not required.

The present method also includes selecting a source of electromagneticradiation, for example, low frequency electromagnetic radiation and/orradio frequency elector magnetic radiation. Further, the method includesselecting treatment parameters for an electromagnetic radiationtreatment session. The treatment parameters include, but are not limitedto, a pulse frequency of the electromagnetic radiation, the pulseduration of the electromagnetic radiation, an electrical current, amagnetic filed density, and a treatment session exposure time.

The electromagnetic radiation treatment regimen also includes initiatingthe electromagnetic radiation treatment session, and applying an amountof electromagnetic radiation from the selected electromagnetic radiationsource(s) to the target area in accordance with the treatment parametersselected.

Additionally, the present method further comprises terminating theelectromagnetic radiation treatment session. After the session isterminated, the present method provides for measuring a response of atleast some of the plurality of target area cells to the electromagneticradiation treatment session, and evaluating the response of theplurality of target area cells measured to the electromagnetic radiationtreatment session. Based upon the response of the target area cellsmeasured, revised treatment parameters may be selected, and one or moresubsequent treatment session may be conducted.

These and other objects, features and advantages of the presentinvention will become clearer when the drawings as well as the detaileddescription are taken into consideration.

BRIEF DESCRIPTION OF THE DRAWINGS

For a fuller understanding of the nature of the present invention,reference should be had to the following detailed description taken inconnection with the accompanying drawings in which:

FIG. 1 is a schematic representation illustrative of one embodiment ofan electromagnetic radiation treatment regimen in accordance with thepresent disclosure.

FIG. 2 is a schematic representation illustrative of one embodiment of alow frequency (LF) electromagnetic radiation treatment regimen inaccordance with the present disclosure.

FIG. 3 is a schematic representation illustrative of one embodiment of aradio frequency (RF) electromagnetic radiation treatment regimen inaccordance with the present disclosure.

FIG. 4 is a schematic representation illustrative of one embodiment of acombined parallel low frequency (LF) and radio frequency (RF)electromagnetic radiation treatment regimen in accordance with thepresent disclosure.

FIG. 5 is a schematic representation illustrative of one embodiment of acombined series low frequency (LF) and radio frequency (RF)electromagnetic radiation treatment regimen in accordance with thepresent disclosure.

FIG. 6 is a schematic representation illustrative of one embodiment of asystem for conducting an electromagnetic radiation treatment session inaccordance with the present disclosure.

Like reference numerals refer to like parts throughout the several viewsof the drawings.

DETAILED DESCRIPTION OF THE PREFERRED EMBODIMENT

The treatment regimen of the present disclosure utilizes electromagneticradiation (“EMR”) to treat cancer cells, or other cells amenable topathological genetic regulations. The method of the present disclosurerepresents an ensemble of subcellular elements targeted substantiallysimultaneously to interfere with a cancer cell's control system, and torestore a normal control system to the cancer cell. More in particular,the present method utilizes both electrical current and magnetic fieldsas significant vehicles of action on specific molecular and atomiccomponents of a cancer cell, such as, the protons and electrons of thecancer cell, to elicit a beneficial therapeutic effect. The presentmethod takes advantage of the significant differences in theelectromagnetic properties of normal and cancer cells. Specifically, thedifferences between the electromagnetic properties of normal cells andcancer cells transcend the molecular realm, and extend into the quantummechanism realm. While the present EMR treatment methodology isdisclosed hereinafter with a primary focus on the treatment of cancercells, it is understood to be within the scope and intent of the presentdisclosure to apply the present EMR treatment regimen to other abnormalcells including, but not limited to, cells affected by infectiousdiseases such as HIV/AIDS, H1N1, etc., which are amenable topathological genetic regulations

The method of the present disclosure provides a significantly greatersafety profile than the previously known methods of treating cancercells, such as, surgery, chemoradiation, and/or pharmaceutical treatmentregimens. The safety of the present method inures from theelectrodynamic differences between the cancer cell and the normal cell,for example, the metabolic rate of the cancer cell is much greater thana normal cell, which plays a role in the safety profile of the presentmethod.

Further, the present treatment regimen can be used to treat abnormalcells associated with the at least the following types of cancer: 1)oral cavity and pharynx; 2) esophagus; 3) stomach; 4) small intestine;5) colon or rectum; 6) liver; 7) pancreas; 8) larynx; 9) lung; 10) skinmelanoma; 11) breast; 12) uterine cervix; 13) ovary; 14) prostate; 15)bladder; 16) non Hodgkin's lymphoma; 17) Hodgkin's disease; 18) multiplemyeloma; 19) leukemia; 20) brain and nervous system; 21) thyroid; 22)eye; 23) kidney and renal pelvis; 24) testis; 25) uterus, corpus; 26)soft tissue; 27) bone; and 28) gallbladder and biliary. As noted above,the present EMR treatment methodology may also be utilized fro thetreatment of other abnormal cells including, by way of example only,cells affected by viral infections resulting from influenza A (“H1N1”),also known as swine flu, human immunodeficiency virus (“HIV”), andacquired immunodeficiency virus (“AIDS”). Implementation of thetreatment regimen of the present disclosure results in an interferencewith the control system of cancer cells, halts the progression of thecancer, and can even prevent the initiation of the infection or cancer.

Cellular Control Systems

The control system of a cell is designated as one of three types: 1)bioproportional control, 2) bioderivative control and 3) biointergralcontrol, each indicative of the operation of the control system inphysical and electrical analysis. Bioproportional control is present ina cancer cells throughout its reproductive activity, and allows forsignificant changes in a normal cell as it transforms into a cancercell. This is not a statistical series of events based on randomness,but, rather, directed events occurring in a specific sequence whichdetermine the survival and development of a cancer cell. Bioderivativecontrol regulates cell division and its underlying DNA processes. Incancer cells, bioderivative control is present and regulates theinitiation, or beginning phase, but not the progression, or final phase.Biointergral control addresses small errors which occur repeatedly overtime. Implementation of the present electromagnetic radiation (“EMR”)treatment regimen introduces deliberate errors into the controlsystem(s) of a cancer cell, to counteract the cell's reproductive andsurvival functions, as discussed in greater detail hereinafter.

Low Frequency (“LF”) Electromagnetic Radiation Treatment

Low frequency (“LF”) electromagnetic radiation is utilized in thepresent EMR treatment regimen to produce a pulsed magnetic field of lowfrequency in a range of about 0.5 to 200 Hertz (“Hz”) resulting in apulsed electric field. The pulsed electric field results in analternating current acting upon the critical membranes of the cell, mostdirectly on the cellular membrane. The LF electromagnetic radiation isachieved through the use of LF coils, which are usually circular ordouble constructed and are designed for to apply LF electromagneticradiation to preselected regions of the body in a similar manner as theRF coils discussed hereinafter. The main effect of the application of LFelectromagnetic radiation is to change the polarization of the membranesof target cancer cells.

The membrane polarization change is a function of the intensity,frequency, and direction of the alternating current generated by themagnetic field described by the following hyperbolic relationship:dB/dt=C·R[1+D/TC]where dB/dt is the rate of change of the magnetic field (B), D is thetime for a magnetic pulse to reach maximum and TC is the canceroustissue's electrical time constant, which is a function of thedielectric, resistive, and magnetic properties of the cancerous tissue.C is a constant for the tissue radius and the magnetic fieldorientation.

Activation of protons by an appropriate magnetic field can increase themembrane potential and augment ATP synthesis, producing increased energyfor the cell. Conversely, deactivation of protons by an appropriatelyoriented magnetic field can decrease or prevent ATP synthesis, and thussignificantly diminish the energy available to a cancer cell.

The specific pathway(s) of electrical current through cancerous tissueis difficult to predict, since the tissue segment contains bloodvessels, connective tissue, etc. However, the present EMR treatmentfocuses the positive polarity of the electric field within the canceroustissue and the opposite, negative polarity of the electric field outsidethe cancer cell to affect the membrane potential. For example, todecrease activity of the membrane, the electric field has a direction ofpositive polarity within the cancerous tissue and negative polarityoutside the cancerous tissue, resulting in a hyperpolarization of themembrane. The frequency, intensity, and direction of the magnetic fieldwill be selected and adjusted based upon the nature and type of targetcancerous tissue.

Radio Frequency (“RF”) Electromagnetic Radiation Treatment

In at least one embodiment, the EMR treatment regimen of in accordancewith the present disclosure comprises applying radio frequency (“RF”)electromagnetic radiation to target cancer cells, in order to produce adirect magnetic field effect on nuclei and electrons in the canceroustissue. More in particular, RF electromagnetic radiation is utilized inthe present EMR treatment regimen to affect ATP synthesis, cytochrome C,protons and electrons of the electron transport chain, and DNAstructure.

A radio frequency electromagnetic radiation coil is utilized both tosupply electromagnetic radiation to affect the nuclei and electrons of atarget cell, as well as to detect nuclear or atomic magnetic signalsgenerated in the cancerous tissue. A receiver is utilized to demodulatethe significant signal from the carrier frequency. The radio frequencypulses are generated with center frequencies, bandwidths, amplitudes andphases being preselected based upon the type of cancerous tissue beingtreated, and its location with the patient's body. More in particular,the bandwidth is selected to correspond to the thickness of thecancerous tissue. The duration or shape of the radio frequency pulserelates to the bandwidth, while the amplitude of the radio frequencypulse determines the intensity of the magnetic field. In at least oneembodiment, the radio frequency pulse envelope can be produced bydigital means.

In at least one embodiment of the present EMR treatment regimen whereinRF electromagnetic radiation is applied, RF electromagnetic radiationcoils are arranged parallel to an axis of the patient, i.e., the coilshave the same axis as that of a portion of the patient's body beingtreated. The coils may be resistive, or superconducting, such as, heliumcooled coils. Implementation of the EMR treatment regimen in accordancewith the present disclosure may require utilization of one or more of avariety of RF electromagnetic radiation coils, including 1) head coil,2) integral body coil, 3) spine coil, 4) neck coil, 5) abdominal coil,6) chest coil, 7) knee coil, 8) shoulder coil, 9) flexible coils, 10)tempermandibular coil, etc. The RF electromagnetic coils may surroundthe entire body or only part of the body, or may be placed next to bodyor body part. Magnetic fields are developed by utilizing at least onecoil, or several sets of coils, one for each spatial dimension, orfunctional initiative. The RF electromagnetic radiation coils may beused individually, collectively, or in groups. Moreover, directedwindings are oriented in three orthogonal directions. RF electromagneticradiation pulses or waves are applied repeatedly in a regulated pulse orwave sequence.

The therapeutic effect of the present EMR treatment is a function of theenergy imparted by the magnetic field produced via the RFelectromagnetic radiation. More specifically, the RF electromagneticradiation excites the atoms or nuclei of the target cells. The durationof excitation of the atoms or nuclei can be determined by reorientingthem under a steady magnetic field by a radio frequency pulse. Forinstance, in a steady magnetic field, a 90° radio frequency pulseexcites the nuclei and pushes the oriented nuclei into the transverse,or perpendicular, plane. The nuclei then return to their originalpositions generated by the steady magnetic field, called relaxing, whichhas a characteristic time constant that defines the duration ofexcitation. The time constant is different for cancerous tissue than forother normal tissues of the body. It also varies for different tissues.Fluids have a relatively long time constant in a range of about1500-2000 ms, water containing tissues have a time constant in a rangeof about 400-1200 ms, and fatty tissues have a relatively short timeconstant in a range of about 100-500 ms.

By implementing the present EMR treatment regimen, it is possible toselectively target protons (H⁺) of protein, fat, carbohydrate, proteinbound water, or bulk water. A frequency selective for RF electromagneticradiation excitation is applied for each of the above entities, and canbe applied for all of them at the same time or in sequence. For example,RF electromagnetic radiation can be used to activate fat or water byselection of the appropriate corresponding frequency. The frequency canbe determined by the Larmor equation. For instance, water protonsprecess 220 Hz faster than fat protons when exposed to a magnetic fluxdensity of about at 1.5 Tesla (“T”). Protons in protein bound water havea resonant frequency which is about 500 to 2500 Hz different from bulkwater proton frequency. However, since protein bound protons and bulkwater protons are in rapid exchange, the excitation can be quicklytransferred from protein bound water to bulk water. Notably, theseexcitation times are increased in the case of cancer cells.

In at least one embodiment, the present EMR treatment regimen comprisesenhancing or doping target tissues, such as cancers or tumors, withgadolinium, to increase the precessing frequency of protons. Otherchemicals may also be utilized to enhance or dope target tissues. Forexample, xenon gas may be used to enhance spin effects by producingxenon in a hyperpolarized form, and causing an increased magnetization.The hyperpolarization can also be produced by rubidium vapour. Forexample, xenon is soluble in blood and has a high affinity for lipids.Rubidium vapour can be excited by a diode laser, and act on theelectrons. After electronic polarization, the xenon nuclei are excitedby contact with the rubidium atoms, and then cooled to xenon ice.

In one further embodiment, photons are utilized to augment the effect ofelectromagnetic radiation on electrons and protons. In one embodiment, aradioactive agent or pharmaceutical, such as technetium (Tc-99), whichproduces high energy photons, e.g., 140 kilo electron volt photons, isutilized. Technetium has a half life of about six hours and can beattached to a molecule which combines with a cancer cell. For instance,in one embodiment, Tc-99 methylene diphosphonate (MDP) can be injectedintravenously and absorbed by, and bound to, bone as a result ofosteoblastic activity caused by metastatic deposition.

Moreover, in at least one embodiment, application of RF electromagneticradiation is repeated at suitable intervals to maintain the excitationfor a considerable period of time. The Larmor frequency (r/2_(π)B) forexcitation of protons (H⁺) increases with an increase of the magneticfield. For example, at 0.15 T the Larmor frequency may be 6.39 megahertz(“mHz”); at 0.5 T, 21.29 mHz; at 1.5 T, 63.87 mHz; at 3.0 T, 127.74 mHz.Cancer cells have increased excitation times compared to normal cells.Thus the excitation duration of protons is appreciably greater when theproton is located in or within the immediate environment of an cancercell. This indicates either an increased binding of the proton, or adecreased threshold, or a changed resonant frequency, in comparison tothe normal cell. The cell's return to normal upon application of thepresent EMR treatment regimen can be observed by the cancer cell'sexcitation time becoming essentially the same as the excitation time ofa normal cell.

Accordingly, the excitation time can also be utilized to measure theprogress of the EMR treatment regimen. For instance, the electromagneticradiation fields generated by the proton are detected via receivercoils. Thus, almost simultaneously with application of the EMR treatmentregimen of the present disclosure, it is possible to measure the realtime effect of the treatment.

Combined LF and RF Electromagnetic Radiation Treatment

In at least one embodiment of the present EMR treatment regimen, LFelectromagnetic radiation is applied in conjunction with RFelectromagnetic radiation as discussed above. Further, in oneembodiment, the RF electromagnetic radiation and LF electromagneticradiation are applied in series, whereas, in at least one furtherembodiment, the RF electromagnetic radiation and LF electromagneticradiation are applied in parallel, or in other words, simultaneously.Appropriate shaped electromagnetic radiation pulses are generated atLarmor or other frequencies, and an alternating magnetic field of LFelectromagnetic radiation is produced. With RF electromagneticradiation, a steady magnetic field is employed.

A variety of known components may be arranged and utilized to producethe magnetic fields required for implementation of the present EMRtreatment regimen to act on the cancerous tissue. For instance, a systemcan be used to generate and apply the required electromagneticradiation. Such a system may include at least a configuration ofdirected windings, drivers, radio frequency electromagnetic radiationgenerators, low frequency electromagnetic radiation generators, poweramplifiers, receiver windings, control electronics, frequency reference,receivers, demodulators, frequency oscillators, digital/analogconverters, filters, mixers, preamplifiers, attenuators, an imagingcomponent consisting of receiver windings and EMR coils, receivers,demodulators and acquisition picture, and a measuring componentconsisting of receiver windings and recorder.

A controller may be utilized to apply the appropriate frequency,duration, intensity, etc., and to drive the currents in windings orcoils, which are directed three dimensionally upon the target tissuedirectly or in conjunction with a steady magnetic field. Theelectromagnetic radiation coils are arranged in different spatial planeswith respect to the target tissue to focus the alternating or pulsedelectromagnetic radiation field to the preselected target cells. Thesetarget cells may be located deep within tissue of the body, or may belocated superficially on the body, such as on the skin. Furthermore, inat least one embodiment, the electromagnetic radiation coils aredisposed or positioned perpendicular to a central axis of the targetcells or tissues. In at least one other embodiment, the electromagneticradiation coils are disposed or positioned parallel to the central axisof the target cells or tissue.

The effectiveness of the electromagnetic radiation coils can also beenhanced in a variety of ways. For example, a ferromagnetic material canbe placed around at least one electromagnetic radiation coil to increasethe effectiveness of the electromagnetic radiation field that coilgenerates. In another embodiment, at least one electromagnetic radiationcoil is superconducting, thereby increasing the effectiveness of thefield generated thereby. Moreover, the electromagnetic radiation fieldproduced by an electromagnetic radiation coil can be focused andintensified by placing magnetic or paramagnetic material within orsurrounding the target are of the body. In one embodiment, the magneticor paramagnetic material is placed in or near the target area byinjection of the material into nearby blood vessels. In anotherembodiment, the magnetic or paramagnetic material is placed externallyto the target region, such as with an external magnetic device.

The frequency range of the electromagnetic radiation coils is either aradio frequency or low frequency. In the case of LF electromagneticradiation coils, the electromagnetic radiation field producespolarizations of membranes in different target regions of the body of apatient depending on the size, orientation and geometry of theelectromagnetic radiation coil with respect to the target area, thestrength of the resultant alternating electromagnetic radiation field,and a frequency with respect to the target area of an alternatingelectromagnetic radiation field.

In the case of RF electromagnetic radiation coils, the electromagneticradiation field produces activation or deactivation of the electrontransport system or electrons or protons of nuclei in cancer cells inthe target area depending on at least a size, orientation and geometryof the electromagnetic radiation coil, the intensity of theelectromagnetic radiation field, and a frequency with respect to thetarget area of the steady state electromagnetic radiation field.

The controller further directs the frequency, duration and magnitudefield in the radio frequency range. The Larmor frequency is thereference for the resonant frequency of the target nuclei. A magneticfield, specifically, a steady state magnetic field produced by a fixedmagnet is utilized in conjunction with RF electromagnetic radiation.Further, X, Y, and Z directed windings are used, and refer to onespatial embodiment of the coils in orthogonal, or perpendicular,orientations. A receiver and a demodulator may be collectively employedto measure the excitation durations of nuclei in the cancerous tissuevia receiver windings. Accordingly, and as noted above, the present EMRtreatment regimen may be utilized both to affect treatment as well as tomeasure the effectiveness of the same.

Effectiveness of Electromagnetic Radiation Treatment

The EMR treatment regimen in accordance with the present disclosurecomprises both an action and a signal. One of the effects ofimplementation of the present EMR treatment regimen is to initiate amemory so that effectiveness can increase over time. For memory to beinitiated, EMR treatment is performed in a rapid sequence of signalswhich correspond to the sequential actions of the control system of thecell. Specifically, the sequential actions resulting from implementationof the present EMR treatment regimen in this manner begin with thecellular or plasma membrane, mitochondrial membrane, and nuclearmembrane microtubules. Although, there are a number of other cellularcomponents involved in the sequence, the affect of the present EMRtreatment on the membranes of cancer cells is sufficient to establishthe initiation of the cellular memory. The conformation of a specificmembrane protein is a component of the memory, but overall memorycorresponds to a dynamic control system in the living cell. To implementmemory, the sequential actions within the control system should be thosefollowed by EMR treatment.

It should be appreciated that implementation of the present EMRtreatment regimen can assume a number of different forms, patterns orintensities depending on the nature of the cell, its location in thebody, the stage of cancer or infection, the type of cancer or infection,etc. More in particular, the electromagnetic radiation field applied, aswell as frequency, intensity, pulse, etc., are all preselected inaccordance with the nature and location of the cancer cells within thepatient's body. When the present EMR treatment regimen is implemented,the memory of the treated cancer cell will correspond to an integrationof control system correction, and repeated treatments will demonstrateincreasing effectiveness.

Animal Tissue Model

An animal tissue model may be utilized to demonstrate the electricalmanifestations of a cancer cell, and its differences from the normalcell. This is important because, with the exception of nerve and musclecells, there is virtually little that is known, studied, or investigatedwith regard to the electrical differences between normal and cancercells.

Thus, the experimental model developed and disclosed herein isstructured to measure electrical properties of the cancer cell, andcompare these to the normal cell, as no such model is known to exist.This experimental model provides support for the science underlying thepresent EMR treatment regimen, and also assists in determining theparameters which would be most effective for the treatment. This modelis developed for the investigation of cancer cells compared to normalcells, and is presented as an illustrative approximation of the resultswhich may be obtained via implementation of the EMR treatment regimen inaccordance with the present disclosure.

To begin, a cancer process is initiated in a cellular population ofseveral thousand cells by utilization of a virus. The tissue can beexcised from the host animal, such as a rat, and placed in a controlledenvironment. Electrodes are placed on or near the infected cellularpopulation to measure electrical changes which emanate directly from thecellular membranes and membrane potentials. These signals are firstamplified and then recorded. The first electrical signal observed willbe a non-periodic oscillation which arises from the cancer process, andis not generated by normal cells. A single component of the oscillationlasts about 250 milliseconds and represents a large depolarization,essentially equal to the magnitude of the resting cellular membranepotential, followed by repolarization and hyperpolarization, wherein thehyperpolarization change lasts about 30 milliseconds.

The observation that this cellular and membrane activity is fromisolated tissue indicates it is not initiated by way of its environment,such as hormones, nerves, etc., but rather is due to the cancerousprocess within the cell. This electrical activity is not present in thenormal cell tissue, as noted above, even if the normal cell tissue isisolated, in the same way, i.e., isolated from the animal in vitro.Accordingly, the foregoing demonstrates that the control system of thecancer cell no longer relies upon an external component, and isindependent of external influence.

In order to substantiate this observation, the cancerous tissue is leftin contact with the animal and surrounding tissue, while recordingduring this same time period. No oscillations are observed. However, ifthe tissue is left in place, but simply isolated chemically orsurgically, the oscillations appear after a lag time of approximately aminute. So that external input to these cells is definitely present andcan prevent the oscillations during this period of time. What is meantby this period of time is that these are the first electrical changesthat are observed by recording in this way. A minute lag time perhapsinvolves the lingering effects of the external input, or the time takenfor the cancer cell's control system to achieve dominance.

This phase in the cancer cell's development is called promotion, and isgenerally accepted to be reversible. The present EMR treatment regimencan be implemented to substitute for external modulation of the cancercell and replace it, to reverse and prevent development of the cancerousprocess to produce, in effect, a benign cancer which does notmetastasize.

The remaining phase of the cancer cell's development is calledprogression and is considered to be irreversible. In the animal tissuemodel, this phase is correlated with an increase in frequency andmagnitude of the oscillations from the cancer cells. More importantly,the hyperpolarization at the termination of the single oscillatoryexcursion is absent. In addition, the oscillations appear spontaneouslyat this time in the intact cancerous tissue. The hyperpolarizationdetermines that there is a single oscillation. In the absence of thehyperpolarization, multiple oscillations, such as a train or complex,occur at a frequency which elevates the complex above baseline, and thispattern is repeated. This indicates that the energy necessary for thisprocess is under the control of the mitochondria, and thehyperpolarization terminates that period of energy production resultingin a single oscillation. Implementation of the present EMR treatmentregimen produces a hyperpolarizing current which would do the same andreverse the process to single oscillations, the promotion phase which isreversible.

To demonstrate these effects in the animal tissue model, acetylcholineis applied and combines with its receptor in the membrane, and decreasesthe membrane potential to initiate the cellular functions. In the nervecell, this would include the action potential, as would also be thecondition in the muscle cell. The effects of other pharmacologicalagents, which combine with protein receptors in the cellular membrane,can also be demonstrated. The effects include transforming the cancercell, as observed by its membrane potential changes, from promotion toprogression, and reversing the cancer cell's development fromprogression to promotion. Thus, not only promotion, but progression maybe reversible upon implementation of the present EMR treatment regimen.

Affects of Electromagnetic Radiation Treatment

Implementation of the EMR treatment regimen as disclosed above producesat least the following two results: 1) restoration of the missingcomponent(s) of the cell's normal control system, and/or impeding theactivity of the cancer cell's control system; and, 2) initiatingapoptosis in cancer cells. An essential element of the control system ofany cell is energy generation, which occurs primarily in themitochondria, and apoptosis, which is also primarily initiated in themitochondria. To elicit the aforementioned results, the present EMRtreatment regimen acts upon at least one of the following: 1) membranes,including cellular, mitochondrial, and nuclear membranes, andparticularly focusing upon the membrane potentials or dipoles; and, 2)molecular or atomic entities, including protons, carbon and nitrogennuclei, the heme group of cytochrome C, protein electron carriers (suchas those of the electron transport chain), ATP synthase, DNA andmicrotubules.

The specific impact of implementation of the present EMR treatmentregimen on the various cellular properties and cellular components isdiscussed in further detail in the following sections.

Membranes—Cellular, Nuclear, Mitochondrial

One result of the EMR treatment regimen of the present disclosure is toaffect a cancer cell by producing a hyperpolarization therein, i.e.,reducing the activity of the cancer cell. Since the cancer cell ishyperactive, or has a higher activity level than that of a normal cell,the present EMR treatment selectively targets and interferes with theincreased activity of cancer cells, thereby minimizing, if noteliminating altogether, any negative impact on normal cells inproximity. Hyperpolarization at critical membranes of a cancer cellslows or prevents growth in the cancer cell, and may ultimately resultin eventual cell death via apoptosis.

On the other hand, the present EMR treatment can also affect cancercells by causing a decrease in a cancer cell's membrane potential, ordepolarization, resulting in a decrease in the functional activity ofthe cell. A directional current in accordance with the present EMRtreatment regimen can selectively depolarize or hyperpolarize thecellular membrane of the cancer cell. The directional current utilizedby the present method has a frequency in the range of about 0.5 Hz to1000 Hz, and in at least one embodiment, in a range of about 0.5 Hz to200 Hz, depending on the type and location of the cell, for example, acancer cell. The frequency of the directional current utilized inaccordance with the present disclosure depends on the time constant ofthe membrane, as well as other factors.

In at least one embodiment, EMR treatment can also change the membranepotential by acting on the voltage gate, such as the Na⁺/K⁺ pump, bychanging the conformation of the Na⁺/K⁺ pump between a linear form,having lower energy, and a circular or twisted form, having higherenergy. The EMR treatment in accordance with the present disclosure canact directly on the cellular membrane of a cancer cell through a currenteffect which then continues to the mitochondrial inner membrane, nuclearmembrane, and microtubule. Such a current effect is produced by lowfrequency (“LF”) Electromagnetic radiation, as explained in greaterdetail hereinafter, and/or it may be produced by an adjunct implanteddevice, also described below.

The present EMR treatment acts on the mitochondria at several molecularand membrane sites, to produce a decrease in metabolism or apoptosis.The present EMR treatment is not structured to immediately destroy thecancer cell, as is the intent of surgery or chemoradiation, but ratherto affect a more gradual and safer, transformation or elimination. EMRtreatment in accordance with the present disclosure accomplishes thesafe transformation or elimination of cancer cells by diminishing ATPproduction and decreasing the energy available to the cancer cell,without affecting the energy of the normal cells. In at least oneembodiment, ATP production and energy in a cancer cell is reduced bychanging the membrane potential of the inner mitochondrial membrane. Inat least one other embodiment, ATP production and energy in the cancercell is reduced by decreasing proton flow.

A change in the membrane potential of a cell can be transmitted from thecellular membrane to the mitochondrial and nuclear membranes. A changein membrane potential, and thus polarization of the membrane, results ina change in level of functional activity of the cell, and a change inenergy generation, or set point. For example, an increase in themembrane potential of a cell decreases cellular function and decreasesmitochondrial energy production. At the mitochondria, a change in theproton gradient across the inner mitochondrial membrane results in achange in the function of the electron transport chain proteins, andtherefore, ATP production, as well as membrane potential, electronpotential, NADPH synthesis, ATP, active transport, and heat production.The foregoing processes affect energy production which is required forthe cancer cell to conduct other cellular processes, such as DNAactivity. Accordingly, a change in the set point and energy productioncorrespondingly produces a change in DNA activity. The present EMRtreatment can thus interrupt DNA activity by hyperpolarizing at leastthe cellular membrane, and substantially, if not completely, inhibit DNAactivity.

One effect of implementation of the present EMR treatment regimen is todecrease the rate of energy production in the cancer cell. More inparticular, upon decreasing the energy production in cancer cells viathe present EMR treatment, any excess energy present in the cell isreleased as heat and/or is stored as useful energy in ATP.

Spin Frequency

As noted above, the present EMR treatment reduces the energy availableto the cancer cell, i.e., decreasing the energy production in cancercells, without significantly interfering with the energy productionmechanism of surrounding normal cells. The present method accomplishesthis by acting on the protons of the membrane constituting the temporaryenergy storage mechanism in a cancer cell, specifically by changing thenatural or resonant frequency of the proton spin via a magnetic field.Alternatively, implementation of the present method acts upon theelectron carrier proteins of the electron transport chain by impingingon the natural or resonant frequency of the carbon or nitrogen nuclei ofthese proteins. Since the velocity of movement of the protein in thecancer cell is higher than in the normal cell, decreasing this velocitywill decrease energy production.

The present EMR treatment acts directly on the carbon and nitrogen atomsand protons of the proteins composing the electron transfer system ofcancer cells. This is accomplished by altering their spin frequency,which decreases the efficiency of electron transport. Further, selectionof the frequency, intensity, and direction of an amount ofElectromagnetic radiation applied to cancer cells, referred to as targetcells herein, in accordance with the present EMR treatment regimenalters the energy level and movement of the protons to decrease ATPproduction of the cancer cell, without significantly affecting thenormal cells. Accordingly, the rate of production of ATP by the cancercell is diminished, while the rate of production of ATP by the normalcell, which is normally less than that of the cancer cell, remainssubstantially unaffected. Moreover, the electrical charges associatedwith ATP and the resulting ADP, AMP, and pyrophosphate, which evolved asenergy rich phosphate bonds, can be broken via implementation of thepresent EMR treatment regimen to reduce the amount of ATP available tothe cancer cell.

In at least embodiment, implementation of the EMR treatment regimen inaccordance with the present disclosure significantly diminishes ATPproduction by affecting the mitochondrial membrane protons. EMRtreatment in accordance with the present disclosure acts directly on theprotons and electron transport proteins to diminish ATP production,instead of blocking it, so as not to significantly affect normal cells.

An increased effect on the electron transport chain proteins is realizedvia utilization of radio frequency (“RF”) electromagnetic radiation, asdiscussed in further detail below. An increase in the spin frequency ofprotons denotes an increase in energy, and a decrease in the spinfrequency represents a decrease in energy. An increase in spin frequencyis accomplished by an application of RF electromagnetic radiation at afrequency greater than the resting spin frequency. Similarly, a decreasein spin frequency is accomplished by the application of RFelectromagnetic radiation having a frequency less than the resting spinfrequency. An increase in spin frequency adds energy to power theelectron transport system, while a decrease in spin frequency slows theelectron transport system.

Additionally, implementation of the present EMR treatment regimen altersthe excitation times of protons within cancer cells in a specifictissue, such as cancer. Specifically, as the present EMR treatmentinterferes with the control system of cancer cells, particularly throughthe application of RF electromagnetic radiation, the cancer cells arereprogrammed to a more normal cell profile. As this occurs, the protonsof the target cells adopt excitation times closer to those of protons innormal cells. Further, the present EMR treatment affects the energymolecules ATP, ADP or AMP to prevent electron transfer from eachmolecule's orbital by causing the electron to fall to a lower energyorbital, thus reducing the energy available to the cell overall.

Upon implementation of the EMR treatment regimen, the electron transportchain system of the target cell releases the energy it has absorbed fromthe EMR field at the end of the transport path, according to thefollowing formula:dE/dxαZ ² ρ/v ²

where dE is the energy released, dx is the length of the pathway, v isthe velocity of the transport system, Z is the charge (proton andelectron) deposited at the molecular end site, and ρ is the chargedensity at the molecular end site. An approximate value for the electronenergy, as an example, is 10 Kilo electron volts (“Kev”), and 17 Kev forthe proton.

The present EMR treatment also acts on protons of proteins and DNA,however, it does not breakup the protein or DNA molecule, rather, thepresent treatment minimizes carrying out of their respective functions.

Cytochrome C

Another way implementation of the present EMR treatment regimen acts tosignificantly reduce the energy available to a cancer cell, withoutsignificantly interfering with surrounding normal cells, is byinterfering with the energy mechanism via magnetic interaction with theheme group of the mitochondrial membrane protein cytochrome C. The hemegroup of cytochrome C comprises iron and, therefore, is capable ofmagnetic manipulation via EMR treatment in accordance with the presentdisclosure. Implementation of the present EMR treatment regimen resultsin magnetization of the iron of the heme group of cytochrome C, whichdisplaces or dislodges cytochrome C from the inner mitochondrialmembrane, thus interfering with the electron transport chain and ATPsynthesis, and ultimately, resulting in apoptosis, or cell death.

Specifically, cytochrome C is loosely held or associated with the innermitochondrial membrane by covalent bonds. EMR treatment in accordancewith the present disclosure provides a torque on the heme group ofcytochrome C by application of a steady magnetic field, and applicationof low frequency (“LF”) electromagnetic radiation vibrates thecytochrome C until it is dislodged and ejected from the membrane. Oncecytochrome C is dislodged from the membrane, the electron transportchain is interrupted and ATP synthesis halts. Accordingly, ejection ofcytochrome C from the membrane causes apoptosis and eventual death ofthe cancer cell. However, disruption of cytochrome C can be accomplishedwithout damage to the normal cells by adjusting the level of lowfrequency (LF) electromagnetic radiation to selectively act only on theincreased activity of the cancer cell's inner mitochondrial membrane.Indeed, a magnetic field of sufficient magnitude could be sufficient forEMR treatment to be successful.

Hydrogen Bonds/DNA

The present EMR treatment also acts directly on DNA molecules to preventthe propagation of cancer cells. As in the case of proteins, EMRtreatment in accordance with the present disclosure does not break upthe DNA molecule, but minimizes its ability to function. For instance,electromagnetic radiation can act on the hydrogen bonds holding togetherbase pairs of DNA. As the hydrogen bonds absorb energy from theelectromagnetic radiation, they become excited, and the excitation ofthe hydrogen bonds can cause the bonds to break. Once some of thehydrogen bonds holding together the strands of DNA are broken, thecancer cells will not be able to replicate, and will eventually die.

In at least one embodiment, implementation of the present EMR treatmentregimen alters the charge distribution along a DNA molecule. By alteringthe charge distribution on a strand of DNA, the function and/or activityof the DNA is modified or nullified. For instance, canceling out apositive charge at a particular location on a DNA molecule can changethe three dimensional conformation of the DNA to an inactive form. Inanother example, EMR treatment in accordance with the present disclosuregreatly reduces the attraction between two poles, thereby changing theshape of the molecule from a circular form to a linear form.

It is also possible to change an inactive protein or DNA molecule intoan active form with via EMR treatment in accordance with the presentdisclosure. For example, adding a positive charge to a neutral pole ofan inactive protein causes it to assume a circular form in which it isfunctional. In another example, if the protein is inactive in the linearform and has negative charges at its poles, it can be made active bychanging one negative pole to have a positive charge, thereby causingthe protein to assume a circular, active form.

Microtubules

The EMR treatment also affects cellular activity of cancer cells throughaction on a cell's microtubules. A change in the membrane potential issignaled to the nucleus, and vice versa, via microtubules that connectthe cellular membrane and nuclear membrane. EMR treatment in accordancewith the present disclosure reduces the formation, growth, and dipolemagnitude of the microtubules. Since microtubules also play an importantrole in mitosis and cell growth, implementation of the present EMRtreatment regimen also prevents mitosis, or delays mitosis, bypreventing or delaying microtubule growth. Further, the present EMRtreatment interferes with and delays movement of motor proteins alongmicrotubules.

Illustrative Electromagnetic Radiation Treatment Regimens

The foregoing presented the details of the mechanics and affects ofimplementation of an electromagnetic radiation (“EMR”) treatment regimenin accordance with the present disclosure. As such, and with thatunderstanding, illustrative examples of various specific EMR treatmentregimens are presented below with reference to the figures presentedherewith.

Electromagnetic Radiation Treatment Regimen

Looking first to FIG. 1, a schematic illustration of an EMR treatmentregimen in accordance with the present disclosure is presented and isgenerally indicated as at 100. To begin, the EMR treatment regimen 100requires identifying 110 a target area on a patient for treatment. Thismay be based upon visual observation, such as the presence of a tumor,lesion, or other externally visible indication of the presence of cancercells. Alternatively, identifying 110 the target area may requirenon-invasive techniques such as optical or sonic imaging, or invasivetechniques, such as, testing of actual tissues samples, in order todetect the presence of cancer cells and define a target area. In atleast one embodiment, the target area may be identified to include thepatient's entire body.

Once the target area has been identified, the EMR treatment regimen 100includes isolating 112 the target area for exposure to electromagneticradiation. Isolating 112 the target area may simply comprise positioningof one or more electromagnetic coils in proximity to the target area. Inat least one embodiment, isolating 112 the target area comprises theplacement of physical barriers between an electromagnetic radiationsource and non-targeted areas of the patient. As one example, a shield,such as a lead shield commonly employed to isolate expose to x-rays, maybe positioned over non-targeted areas of the patient's body. Of course,in the event the target area is identified to comprise the patient'sentire body, the step of isolated 112 the target area is not required orperformed.

The EMR treatment regimen 100 as illustrated in FIG. 1 further comprisesselecting 113 a source of electromagnetic radiation. In at least oneembodiment, and as presented in the illustrative embodiment of FIG. 2, alow frequency (“LF”) electromagnetic radiation source is provided,whereas in the embodiment illustrated in FIG. 3, a radio frequency(“RF”) electromagnetic radiation source is provided. In the furtherillustrative embodiments of FIGS. 4 and 5, both LF and RFelectromagnetic radiation sources are provided.

The present EMR treatment regimen 100 further comprises selecting 120one or more treatment parameters which serve to control the amount ofelectromagnetic radiation to be applied to the target area of thepatient. As previously discussed, the parameters which affect the amountof electromagnetic radiation include the pulse frequency ofelectromagnetic radiation, the pulse duration of electromagneticradiation, the amount of electrical current induced by theelectromagnetic radiation, the magnetic flux density, and the treatmentsession exposure time. Each of these parameters is discussed in furtherdetail below with respect to the various types of electromagneticradiation which may be applied.

Following the selection of one or more EMR treatment parameters, thepresent EMR treatment regimen 100 further comprises initiating 121 anEMR treatment session. More in particular, each EMR treatment sessionincludes applying 122 an amount of EMR to the target area. Of course, itwill be appreciated that the amount of EMR actually applied to thetarget area is a function of the pulse frequency, the pulse duration,and the treatment session exposure time, as noted above. Once thedesired amount of EMR has been applied to the target area, the presentEMR treatment regimen 100 includes terminating 123 the EMR treatmentsession.

In order to determine the effectiveness of the EMR treatment session,the EMR treatment regimen 100 of the illustrative embodiment of FIG. 1further comprises measuring 124 a response of at least some of thetarget area cells to the EMR treatment session. As noted above, theexcitation duration of protons is appreciably greater when the proton islocated in or within the immediate environment of a cancer cell. Thus, acell's return to a normal state following EMR treatment can be observedby the cancer cell's excitation time becoming essentially the same asthe excitation time of a normal cell. Accordingly, the excitation timemay be utilized to measure the progress of the EMR treatment regimen100. In at least one embodiment, the electromagnetic radiation fieldsgenerated by the proton are detected via receiver coils. In one furtherembodiment, a receiver and a demodulator are collectively employed tomeasure the excitation durations of nuclei in the cancerous tissue viareceiver windings. Thus, almost simultaneously with application of theEMR treatment regimen 100, measuring 124 the real time effect of thetreatment is possible.

The EMR treatment regimen 100 of the embodiment of FIG. 1 furtherincludes evaluating 125 the response of at least some of the target areacells to the EMR treatment sessions. This evaluation is conducted via acomparison of the measured properties of the target area cells prior toapplying 122 the amount of EMR to the target area with the measuredproperties of the target area cells after applying 122 the amount of EMRthereto. The properties of the target area cells may be measured by avariety of techniques, including MRI and/or blood analysis. For example,blood analysis may be performed to detect the presence of any of anumber of serum tumor markers including, but not limited to:carcinoembryonic antigens; CA 125; elevated serum acid phosphatase;human chorionic gonadotropin; α-fetoprotein; β₂-microglobulin; andlactic dehydrogenase.

Low Frequency Electromagnetic Radiation Treatment Regimen

FIG. 2 is illustrative of one embodiment of an EMR treatment regimen 100in accordance with the present disclosure utilizing a low frequencyelectromagnetic radiation source. As before, the EMR treatment regimen100 requires identifying 110 a target area on a patient for treatment.Once again, upon identifying 110 the target area, the EMR treatmentregimen 100 includes isolating 120 the target area for exposure toelectromagnetic radiation. The EMR treatment regimen 100 as illustratedin FIG. 2 further comprises providing 114 a low frequencyelectromagnetic radiation source.

The embodiment of the EMR treatment regimen 100 illustrated in FIG. 2further comprises selecting 130 one or more initial treatment parameterswhich effectively control the amount of low frequency electromagneticradiation to be initially applied to the target area of the patient. Aspreviously discussed, the treatment parameters which affect the amountof electromagnetic radiation include the pulse frequency, the pulseduration, the amount of electrical current induced by theelectromagnetic radiation, the magnetic flux density, and the treatmentsession exposure time.

In at least one embodiment of the present EMR treatment regimen 100, thetreatment parameters selected include one or more of the following. Inat least one embodiment, a pulse frequency of the low frequencyelectromagnetic radiation source is selected to be in a range of about0.5 hertz to 1000 hertz, and in at least one further embodiment, thepulse frequency is selected in a range of about 0.5 hertz to 200 hertz.A pulse duration in a range of less than or equal to about 300milliseconds is selected in at least one embodiment of the present EMRtreatment regimen. Further, an electrical current in a range of about0.1 milliampere to 1 ampere may be selected. In addition, in accordancewith at least one embodiment of the present disclosure, a magnetic fluxdensity in the range of about 0.5 tesla to 10 tesla may comprise one ofthe selected treatment parameters. At least one embodiment of thepresent EMR treatment regimen also includes selecting a treatmentexposure time to be in a range from a minimum treatment exposure time ofabout five (5) seconds to a maximum treatment exposure time of aboutthirty (30) minutes. Of course, it is understood to be within the scopeand intent of the present disclosure for additional treatment parametersto be selected and/or to select one or more of the treatment parametersidentified above in an operating range which is different than theoperating ranges identified for the illustrative examples presentedherein.

Following the selection of one or more initial low frequency EMRtreatment parameters, the embodiment of the EMR treatment regimen 100 inaccordance with FIG. 2 further comprises initiating 131 an initial lowfrequency EMR treatment session. More in particular, the initial lowfrequency EMR treatment session includes applying 132 an initial amountof low frequency EMR to the target area. Of course, it will beappreciated that the amount of EMR actually applied to the target areais a function of the pulse frequency, the pulse duration, and thetreatment session exposure time, as noted above. Once the desired amountof EMR has been applied to the target area, the present EMR treatmentregimen 100 includes terminating 133 the EMR treatment session.

As before, in order to determine the effectiveness of the initial lowfrequency EMR treatment session, and in order to allow for adjustment ofone or more treatment parameters as may be warranted in order tomaximize the effectiveness of the present EMR treatment regimen 100, theillustrative embodiment of the EMR treatment regimen 100 of FIG. 2further comprises measuring 134 a response of at least some of thetarget area cells to the initial low frequency EMR treatment session.Measuring 134 the response of the target area cells is performed in themanner discussed above with respect to FIG. 1. Similarly, the EMRtreatment regimen 100 of the embodiment of FIG. 2 further includesevaluating 135 the response of at least some of the target area cells tothe initial low frequency EMR treatment session in the manner discussedabove with respect to FIG. 1.

The illustrative embodiment of the low frequency EMR treatment regimen100 of FIG. 2 further comprises the steps of: selecting 130′ subsequenttreatment parameters for one or more subsequent low frequency EMRtreatment session(s); initiating 131′ a subsequent low frequency EMRtreatment session; applying 132′ a subsequent amount of low frequencyEMR to the target area; terminating 133′ the subsequent low frequencyEMR treatment session; measuring 134′ the response of at least some ofthe target area cells to the subsequent low frequency EMR treatmentsession; and, evaluating 135′ the response of at least some of thetarget area cells to the subsequent low frequency treatment session. Itwill be appreciated that each of the aforementioned subsequent steps isconducted in a manner that equates to the corresponding initial steps131-135 discussed above, with the exception of selecting 130′ thesubsequent treatment parameters, which will be informed by the initialmeasuring 134 and evaluating 135 steps, or by the immediately precedingsubsequent measuring 134′ and evaluating 135′ steps.

Radio Frequency Electromagnetic Radiation Treatment Regimen

One embodiment of an EMR treatment regimen 100 utilizing a radiofrequency electromagnetic radiation source in accordance with thepresent disclosure is depicted in FIG. 3. As with the previouslydisclosed embodiments, the EMR treatment regimen 100 of FIG. 3 includesidentifying 110 a target area on a patient for treatment. Once again,upon identifying 110 the target area, the EMR treatment regimen 100includes isolating 112 the target area for exposure to electromagneticradiation. The EMR treatment regimen 100 as illustrated in FIG. 3further comprises providing 114 a radio frequency electromagneticradiation source.

As disclosed above, when utilizing a radio frequency electromagneticradiation source, a magnetic source is also provided, such as isindicated in FIG. 3 at 115, in proximity to the target area cells. Inone embodiment, a magnetic or paramagnetic material is placed in or nearthe target area by injection of the material into nearby blood vessels.In another embodiment, the magnetic or paramagnetic material is placedexternally to the target region, such as with an external magneticdevice. Once in position, the magnetic or paramagnetic material isresponsible for generating 116 a magnetic field proximate the targetarea cells.

Following the generation of the magnetic field, the radio frequency EMRtreatment regimen 100 as illustrated in FIG. 3 essentially proceeds in asimilar manner as the low frequency EMR treatment regimen 100 asillustrated in FIG. 2. Specifically, the radio frequency EMR treatmentregimen 100 of FIG. 3 comprises: selecting 140 initial treatmentparameters for an initial radio frequency EMR treatment session;initiating 141 an initial radio frequency EMR treatment session;applying 142 an initial amount of radio frequency EMR to the targetarea; terminating 143 the initial radio frequency EMR treatment session;measuring 144 the response of at least some of the target area cells tothe initial radio frequency EMR treatment session; and, evaluating 145the response of at least some of the target area cells to the initialradio frequency treatment session.

FIG. 3 is also illustrative of the further steps of: selecting 140′subsequent treatment parameters for one or more subsequent radiofrequency EMR treatment session(s); initiating 141′ a subsequent radiofrequency EMR treatment session; applying 142′ a subsequent amount ofradio frequency EMR to the target area; terminating 143′ the subsequentradio frequency EMR treatment session; measuring 134′ the response of atleast some of the target area cells to the subsequent radio frequencyEMR treatment session; and, evaluating 135′ the response of at leastsome of the target area cells to the radio frequency treatment session.

Similar to the low frequency EMR treatment regimen 100, the step ofselecting 140′ the subsequent treatment parameters, which will beinformed by the initial measuring 144 and evaluating 145 steps, or bythe immediately preceding subsequent measuring 144′ and evaluating 145′steps.

Combined LF/RF Electromagnetic Radiation Treatment Regimen

FIGS. 4 and 5 are illustrative of embodiments of EMR treatment regimens100 in accordance with the present disclosure in which both lowfrequency and radio frequency electromagnetic radiation are utilized.More in particular, FIG. 4 presents an EMR treatment regimen 100 whereinlow frequency electromagnetic radiation is applied to the target area ofthe patient in parallel with the application of radio frequencyelectromagnetic radiation, essentially simultaneously. In thealternative embodiment of FIG. 5, the EMR treatment regimen 100comprises the application of low frequency electromagnetic radiationfollowed by radio frequency electromagnetic radiation to the target areaof the patient, in a series arrangement. Of course, it is within thescope and intent of the present disclosure for an EMR treatment regimen100 to comprise radio frequency electromagnetic radiation followed bylow frequency electromagnetic radiation, as well as series/parallelapplications of the same. Further, in a series arrangement, theapplication of low (or radio) frequency electromagnetic radiation may beimmediately followed by radio (or low) frequency electromagneticradiation, or there may be a rest period between applications, whereinthe rest period may be minutes, hors, or even days.

Looking to FIG. 4, the combined EMR treatment regimen comprises thesteps of identifying 110 a target area, isolating a target area 112,providing 114 an electromagnetic radiation source, providing a magneticsource 115, and generating 116 a magnetic field, which are eachperformed in a manner similar to that described above with regard to theembodiments disclosed in FIGS. 1 through 3.

Next, FIGS. 4 and 5 illustrate the EMR treatment regimens 100 compriseselecting 150, 160 treatment parameters for low frequency EMR treatmentsessions and radio frequency EMR treatment sessions, respectively. Asfurther illustrated in FIGS. 4 and 5, the step of selecting 150, 160treatment parameters includes selecting 151, 161 a pulse frequency,selecting 52, 162 pulse duration, selecting 153, 163 an electricalcurrent, selecting 154, 164 a magnetic flux density, and selecting 155,165 an exposure time.

Once the treatment parameters have been selected, the EMR treatmentregimens 100 of FIGS. 4 and 5 include applying 156, 166 and amount oflow frequency EMR and radio frequency EMR, respectively. The step ofapplying 156, 166 the low and radio frequency EMR occurs essentiallysimultaneously in the parallel configuration of FIG. 4, and one afterthe other in the series configuration in the illustrative embodiment ofFIG. 5. The EMR treatment regimens 100 of the embodiments of FIGS. 4 and5 further comprise terminating 157, 167 the application of low and radiofrequency EMR, respectively.

As in the preceding embodiments, the EMR treatment regimens 100 of theillustrative embodiments of FIGS. 4 and 5 further comprise evaluation170 the response of at least some of the target area cells to the lowfrequency EMR and radio frequency EMR treatment sessions.

FIG. 6 is a schematic representation of system 10 for conducting an EMRtreatment regimen in accordance with the present disclosure. More inparticular, the system 10 comprises a controller 20, which is utilizedfor the selection of the treatment parameters for any particulartreatment sessions. Further, the system 10 includes a source of lowfrequency electromagnetic radiation 30 and a source of radio frequencyelectromagnetic radiation 40. A magnetic source 50 is included forutilization in a radio frequency EMR treatment session.

FIG. 6 further illustrates that the source of low frequency EMR 30,radio frequency EMR 40, and the magnetic source 50 are each disposedproximate at least a portion of the patient, i.e., the target area.Additionally, the system 10 comprises at least one detector 60, which isalso disposed proximate the patient, the detector 60 being operative tomeasure a response of at least some of the cells in the target area toEMR treatment, for evaluation by treating physician/technician.

Early Detection of Cancer

The detection of cancer can come relatively late in its development. Thepresent EMR treatment regimen offers two solutions to this problem.First, the safety profile of the EMR treatment permits its use without adefinitive diagnosis. Second, detection of the excitation signals ofcancer cells allow an earlier diagnosis via implementation of the EMRtreatment regimen of the present disclosure than with previously knownmethods.

The detection of cancer is very difficult before one gram of tumor cellsis present, which represents about one billion cells, and 30 doublingsin volume. Ten further doublings in volume would represent about onekilogram of these tumor cells, which could be lethal. Thus cancer cellsmay be able to metastasize prior to detection. This also means thattumor study occurs over a late, relatively short period of total growth.Because of its safety profile, the present EMR treatment regimen may beutilized when cancer is possible, but not certain, to detect and treatthe cancer cells.

Portable Adjunct Treatment Device

A supplementary treatment may be implemented between EMR treatments viaan implanted electrical device. Such an adjunct treatment device mayconsist of a microcomputer controlled electrical generator implantedbeneath the skin in the region of a cancerous tissue or organ.Electrical connections are positioned between the generator to anelectrode placed approximately in the center of the cancerous tissue,and another electrode placed beyond the limit, or on the periphery ofthe cancer cells. The electrodes may be placed in or near the cancercells or cancerous tissue, or on the skin adjacent to this tissue. In atleast one embodiment, the electrodes are placed to maximize the currentreaching the cancer cells. The polarity of the electrodes would beeither positive or negative, determining the direction of the electricfield or the current. A positive polarity of an electrode disposed inthe interior of cancerous tissue would lead to a decrease in malignancy.

This adjunct treatment device may comprise a small battery poweredgenerator with microcomputer, which can be attached by various means toparts of the body or clothing, and worn comfortably by the patientthroughout the day or evening involving usual activities or sleep.Alternatively, the device can be implanted in or near cancerous tissue.Such a device is intended as an adjunct to EMR treatment in accordancewith the present disclosure, and can be activated for periods of timebetween EMR treatments. The current, frequency, and other parameters areadjusted to meet the needs of the patient and type of character of thecancer cell, primarily to depolarize or hyperpolarize the membranepotentials. In one embodiment, the positive pole is placed in theapproximate center of the mass of cancerous tissue, and the negativepole peripherally or externally thereto.

Since many modifications, variations and changes in detail can be madeto the described preferred embodiment of the invention, it is intendedthat all matters in the foregoing description and shown in theaccompanying drawings be interpreted as illustrative and not in alimiting sense. Thus, the scope of the invention should be determined bythe appended claims and their legal equivalents.

Now that the invention has been described,

What is claimed is:
 1. A method of treating cancer cells withelectromagnetic radiation comprising the steps of: identifying a targetarea for treatment comprising a plurality of target area cells, whereinat least some of the target area cells comprise cancer cells, isolatingthe target area from surrounding areas, providing at least one magneticsource, applying a magnetic field affecting at least some of theplurality of target area cells, selecting low frequency treatmentparameters for a low frequency electromagnetic radiation treatmentsession, selecting radio frequency treatment parameters for a radiofrequency electromagnetic radiation treatment session, applying anamount of low frequency electromagnetic radiation from a low frequencyelectromagnetic radiation source to the target area in accordance withthe low frequency treatment parameters, applying an amount of radiofrequency electromagnetic radiation from a radio frequencyelectromagnetic radiation source to the target area in accordance withthe radio frequency treatment parameters, terminating the application ofthe low frequency electromagnetic radiation to the target area,terminating the application of the radio frequency electromagneticradiation to the target area, and measuring a response of at least someof the cancer cells in the target area to the low frequencyelectromagnetic radiation treatment session and the radio frequencyelectromagnetic radiation treatment session.
 2. The method as recited inclaim 1 further comprising separately applying the amount of lowfrequency electromagnetic radiation to the target area and applying theamount of radio frequency electromagnetic radiation to the target areain a series treatment regimen.
 3. The method as recited in claim 1further comprising concurrently applying the amount of low frequencyelectromagnetic radiation to the target area and applying the amount ofradio frequency electromagnetic radiation to the target area in aparallel treatment regimen.
 4. The method as recited in claim 1 whereinthe low frequency electromagnetic radiation treatment session reduces amicrotubule growth rate in at least some of the cancer cells in thetarget area.
 5. The method as recited in claim 1 wherein the radiofrequency electromagnetic radiation treatment session initiatesapoptosis in at least some of the cancer cells in the target area. 6.The method as recited in claim 1 wherein the radio frequencyelectromagnetic radiation treatment session reduces ATP production in atleast some of the cancer cells in the target area.
 7. The method asrecited in claim 1 wherein each of the low frequency treatmentparameters and the radio frequency treatment parameters comprise atleast one of a pulse duration, an electrical current, a magnetic fluxdensity, or a treatment session exposure time.
 8. The method as recitedin claim 7 wherein the low frequency treatment parameters furthercomprise selecting a pulse frequency in a range of about 0.5 hertz to1000 hertz.
 9. The method as recited in claim 7 further comprisingselecting the pulse duration in a range of less than or equal to about300 milliseconds.
 10. The method as recited in claim 7 furthercomprising selecting the electrical current in a range of about 0.1milliampere to 1 ampere.
 11. The method as recited in claim 7 furthercomprising selecting the magnetic flux density in the range of about 0.5tesla to 10 tesla.
 12. The method as recited in claim 7 furthercomprising selecting the treatment exposure time to be in a range fromabout five seconds to about thirty minutes.
 13. A method of treatingcancer cells with electromagnetic radiation comprising the steps of:identifying a target area for treatment comprising a plurality of targetarea cells, wherein at least some of the target area cells comprisecancer cells, isolating the target area from surrounding areas,providing at least one magnetic source, generating a magnetic fieldaffecting at least some of the plurality of target area cells, selectinginitial low frequency treatment parameters for an initial low frequencyelectromagnetic radiation treatment session, selecting initial radiofrequency treatment parameters for an initial radio frequencyelectromagnetic radiation treatment session, applying an initial amountof low frequency electromagnetic radiation from a low frequencyelectromagnetic radiation source to the target area in accordance withthe initial low frequency treatment parameters, applying an initialamount of radio frequency electromagnetic radiation from a radiofrequency electromagnetic radiation source to the target area inaccordance with the initial radio frequency treatment parameters,terminating the application of the low frequency electromagneticradiation to the target area, terminating the application of the radiofrequency electromagnetic radiation to the target area, measuring aresponse of at least some of the cancer cells in the target area to theinitial low frequency electromagnetic radiation treatment session andthe initial radio frequency electromagnetic radiation treatment session,evaluating the measured response of the cancer cells in the target areato the initial low frequency electromagnetic radiation treatment sessionand the initial radio frequency electromagnetic radiation treatmentsession, selecting subsequent low frequency treatment parameters for asubsequent low frequency electromagnetic radiation treatment session,selecting subsequent radio frequency treatment parameters for asubsequent radio frequency electromagnetic radiation treatment session,initiating the subsequent low frequency electromagnetic radiationtreatment session, initiating the subsequent radio frequencyelectromagnetic radiation treatment session, applying a subsequentamount of low frequency electromagnetic radiation from the low frequencyelectromagnetic radiation source to the target area in accordance withthe subsequent low frequency treatment parameters, applying a subsequentamount of radio frequency electromagnetic radiation from the radiofrequency electromagnetic radiation source to the target area inaccordance with the subsequent radio frequency treatment parameters,terminating the subsequent low frequency electromagnetic radiationtreatment session, terminating the subsequent radio frequencyelectromagnetic radiation treatment session, measuring a response of atleast some of the cancer cells in the target area to the subsequent lowfrequency electromagnetic radiation treatment session and the subsequentradio frequency electromagnetic radiation treatment session, andevaluating the measured response of the cancer cells in the target areato the subsequent low frequency electromagnetic radiation treatmentsession and the subsequent radio frequency electromagnetic radiationtreatment session.
 14. The method as recited in claim 13 whereinmeasuring the response of at least some of the cancer cells in thetarget area comprises capturing at least one image of the target area bymagnetic resonance imaging.
 15. The method as recited in claim 13wherein the response of at least some of the cancer cells in the targetarea is a change in a cell growth rate.
 16. The method as recited inclaim 13 wherein the low frequency electromagnetic radiation sourcecomprises at least one electromagnetic coil.
 17. The method as recitedin claim 13 wherein the magnetic field comprises a steady state magneticfield.
 18. The method as recited in claim 13 wherein the magnetic fieldcomprises a pulsed magnetic field.
 19. The method as recited in claim 13further comprising doping the target area with an amount of a magneticsubstance to enhance the efficiency of the radio frequencyelectromagnetic radiation treatment session, wherein the magneticsubstance is independent of the at least one magnetic source.